Intramuscular energy sources in dogs during physical work

Three groups of dogs were run under different experimental conditions characterized by varying the work load or the running time. Lipid and glycogen analyses were carried out on biopsy specimens from the biceps femoris muscle before and after exercise. In addition, arterial and venous triglycerides and free fatty acids were determined on plasma samples from one group of dogs that had been previously catheterized. Under the conditions of these experiments, results revealed: (1) plasma triglycerides did not contribute significantly to the energy supply for muscle contraction; (2) plasma free fatty acid efflux into muscle was increased during mild exercise but significantly lowered during heavy exercise; (3) exercise did not affect the phospholipid level or its composition in the muscle; and (4) muscle triglyceride levels may increase, decrease, or remain unchanged, depending upon the work load imposed by the exercise.     

External respiration, gas exchange and blood acid-base status in dogs with hyperthermia

Experiments on dogs have shown that hyperthermia intensifies respiration, increases oxygen consumption, induces pronounced discrepancy of the alveolar ventilation to carbon dioxide elimination, severe hypocapnia and decompensated respiratory alkalosis.     

Effect of hyperthermia on the cardio- and hemodynamics and acid-base balance of the blood in dogs

The effect of severe hyperthermia on the circulatory function was studied in dogs. Arterial pressure was maintained at the normal level, cardiac output increased at the core temperature of about 40 degrees C. An abrupt fall of the arterial pressure and cardiac output was observed at the rectal temperature of about 41 degrees C. The results suggest that a decrease in the cardiac output during severe hyperthermia is due to the fall of the central venous pressure and to the increase of the vascular compliance.     

Humoral mechanisms in the regulation of work hyperthermia

Thermal reactions were investigated in rabbits: blood plasma donors running on treadmill to exhaustion and resting blood plasma recipients. Blood plasma was infused in the ear's vein and in the third brain ventricle cavity. Small elevation of body cork temperature (0.3-0.4 degree C) with the latent period 40-50 min was found on plasma infusion in the ear's vein of recipient. Plasma perfusion through the third brain ventricle of the recipient caused two peaks of nearly the same amplitude (0.8-1.0 degrees C) in body core temperature. The second peak, which was registered in 12-15 min after the perfusion began, was induced, as the authors suggest, by the accumulation of "work factor" of thermoregulation in donor's plasma during muscular work. Humoral regulation of working hyperthermia is discussed.     

Regional distribution of cerebral blood flow during exercise in dogs

This study was performed to determine whether exercise produces vasodilatation in regions of the brain that are associated with motor functions despite the associated vasoconstrictor effect of hypocapnia. Total and regional cerebral blood flow (CBF) were measured with microspheres in dogs during treadmill exercise of moderate intensity. Flow was also measured at rest after stimulation of ventilation with doxapram. During moderate exercise, total CBF was not changed significantly, but regional flow was increased in structures associated with motor-sensory control; blood flow to motor-sensory cortex, neocerebellar and paleocerebellar cortex, and spinal cord increased 30 +/- 7%, 39 +/- 8%, and 29 +/- 4%, respectively (P less than 0.05). After doxapram, which increased arterial blood pressure and decreased arterial PCO2 to levels similar to those during exercise, total CBF decreased and there was no redistribution of CBF. These results indicate that exercise in conscious dogs increases blood flow in regions of the brain associated with movement despite the associated vasoconstrictor stimulus of arterial hypocapnia. Thus, during exercise, local dilator influences that presumably result from increases in metabolism predominate over a potent constrictor stimulus in regulation of cerebral vascular resistance.     

Effect of nitric oxide synthase inhibition on regional blood flow during hyperthermia

The loss of compensatory splanchnic vasoconstriction during hyperthermia was assessed in rats after administration of either 0, 10, 30, or 100mg/kg N(w)-nitro-L-arginine methyl ester,L-NAME. Rectal temperature (T(re)), heart rate (HR), mean arterial blood pressure (MAP), breathing frequency (BF), and renal, mesenteric and caudal blood flows (Q(R), Q(M) and Q(C)) were measured until irreversible cardiovascular collapse occurred. HR, MAP and BF increased as T(re) rose to 42 degrees C, then fell as circulatory collapse occurred. As dose increased T(re) at collapse decreased. Q(M) decreased until a T(re) of 41.5-42 degrees C and then increased. Q(R) and Q(C) were unaffected by either hyperthermia orL-NAME. Inhibition of NO synthase did not prevent the circulatory collapse of heatstroke; the higher doses ofL-NAME may have exacerbated the onset of circulatory failure.